This study is prompted by recent clinical evidence implicating transient upper airway obstruction as a cause of potentially fatal cardiorespiratory disturbance during sleep. Such evidence suggests a possible mechanism which may be etiologically significant in the Sudden Infant Death Syndrome (SIDS). In this regard few controlled laboratory investigations have considered the possibility of abnormal laryngeal closure. The broad intent of this on-going project is to 1) neurophysiologically define the central organization of the laryngeal adductor reflexes with respect to a) protective glottic closure, b) laryngeal spasm; 2) select, by means of such accumulated data, the animal model most analogous to the human being in its central organization of laryngeal reflexes; 3) identify patterns of laryngeal reflex development with respect to excitatory and inhibitory elicitations in an attempt to describe those factors of possible etiologic significance appropriate to the time-course of greatest risk in SIDS; 4) quantitate neurophysiologically those ventilatory conditions which might modify or greatly exaggerate those abnormal reflex behaviors which possess potential lethality to the organism itself; and 5) confirm by alternate experimental methods, if possible, those data etiologically significant to SIDS.